1. Field of the Invention
This invention relates generally to a method to treat sphincters, and more particularly to a method to treat esophageal sphincters in mammalian patients as a remedy for Gastroesophageal disease.
2. Prior Art
Gastroesophageal reflux disease (GERD) is a disorder of the lower esophageal sphincter which allows stomach contents to reverse flow into the distal portion of the esophagus during digestion. Complications associated with GERD include heartburn, pulmonary disorders, chest pain, esophageal ulcers, esophagitis, Barrett's esophagus, and esophageal carcinoma.
Treatments for GERD include prescribed acid blockers for limiting gastric production of acid and acid neutralizers. The relief is generally short-term, and the drugs alleviate symptoms of GERD without correcting the underlying dysfunction of the esophageal sphincter.
Various surgical procedures have been in use to correct GERD. In one surgical procedure, Nissen fundoplication, a portion of the gastric fundus is wrapped around the esophagus. The wrapped gastric fundus applies pressure to the esophagus to limit reverse flow of the stomach contents into the esophagus. All the surgical options require a large incision to expose the stomach and the lower esophagus. In laparoscopic procedures, a plurality of smaller incisions are formed in the abdominal wall to insert instruments into the body of the patient. Surgical procedures are expensive and can require significant amounts of recovery time.
Other surgical procedures, such as those disclosed in U.S. Pat. No. 5,403,326 and in U.S. Pat. No. 5,571,116, use surgical staples to secure the fundus of the stomach and the lower esophagus. Staples however, tend to concentrate stresses and could allow for tearing or necrosis of tissue. Movement of the stapled patient also contributes to staple damage. Such rigid instruments are inserted into the operative field with trocar type devices which make abdominal wall penetrations. The abdominal wall penetrations increase the risk of post-operative hernia, accidental organ perforation, or other drawbacks associated with surgical procedures.
Angelchik's U.S. Pat. No. 4,271,827 describes a sutureless procedure for treating GERD when the esophageal junction is positioned above the diaphragm. In this invention a C-shaped cushion prosthesis is disposed about the distal esophagus. The prosthesis prevents motion of the esophagus with respect to the diaphragm. It is not meant to aid the esophageal sphincter in its operation by decreasing the diameter of the esophageal sphincter. The inside diameter of the prosthesis corresponds to the normal outside diameter of the distal esophagus.
Edwards' U.S. Pat. No. 6,044,846 describes a method of treating a sphincter with a catheter that delivers energy to tissue. The energy delivery device has a tissue piercing distal end. Energy is delivered to the sphincter tissue to create necrosis in the sphincter to reduce sphincter relaxation. It does not direct bulk or thicken sphincter tissue.
U.S. Pat. No. 6,251,064 to Silverman et al. describes an implant for treatment of sphincters that involves formation of a solid in situ by precipitation. The implant does not contain functionality and cannot bond to tissue or form a solid implant through polymerization.
Klein's U.S. Pat. No. 6,277,392 describes a tissue augmentation implant for treatment of GERD. The implant is composed of particulate suspended in a liquid carrier. The implant differs from the present invention in that it does not form a solid in the body.
Dittgen et al.'s U.S. Pat. No. 6,303,137 describes an implant that forms a coagulant in situ due to its insolubility in water. The described precipitation reaction provides a solid implant, but differs from the present invention in that the functional end groups of the implant do not form bonds with the patient's tissue.
All of the above inventions differ from the present invention in that the present invention seeks to increase the functionality of the esophageal sphincter by bonding to and bulking the tissue of the lower esophageal sphincter. The tissue bulking increases the tension in the sphincter, creating increased resistance to reflux. The tissue bonding prevents erosion of the tissue around the implant and thus prevents loss of the implant.
It is thus an object of the present invention to provide a Gastroesophageal treatment which overcomes the deficiencies of the prior art, and improving upon them to provide an improved method for treating a mammalian lower esophageal sphincter while reducing the frequency and quantity of reflux to which it is subject.
It is a further object of the present invention to provide a device and method to bulk sphincter tissue and to minimize injury to a mucosal layer of the sphincter.
It is yet another object of this invention to provide a method to controllably increase the bulk of a sphincter without creating a permanent impairment of the sphincter's ability to achieve a physiologically normal state of closure.
It is another object of this invention to provide a method to create a tightening of a sphincter without permanently damaging anatomical structures near the sphincter.
It is still yet another object of this invention to provide a method for controllably increasing the volume and geometry of a lower esophageal sphincter to reduce the frequency and quantity of stomach reflux.
It is yet a further object of this invention to provide an implant that forms a solid by self-polymerization within the patient's body, with no loss of water with the injectate of the present invention by precipitation or otherwise, to create an implant of known and constant and hence accurate volume, where the implant bonds to tissue at the implant site, and is resistant to absorption by the patient's body. The implant being the volume of the injectate.